IRAK1 and infection: These same data suggest that a significant pathological upregulation of NF-kB (p50/p65)–miRNA-146a signaling coupled to downregulation of pathogenic mRNA targets such as IRAK and CFH may directly contribute to altered innate-immune or inflammatory responses in both viral- and prion-mediated infections, features that also accompany progressive, irreversible inflammatory neurodegeneration in a surprisingly wide range of human brain diseases including AD and PrD and in murine transgenic models for these diseases.